LncRNA SNHG17 regulates cell proliferation and invasion by targeting miR-338-3p/SOX4 axis in esophageal squamous cell carcinoma.

Small nucleolar RNA host gene 17 (SNHG17), a novel functional long noncoding RNA, has been demonstrated to play an essential role in the oncogenesis of several tumors. However, for esophageal squamous cell carcinoma (ESCC) the expression pattern and detailed function of SNHG17 are largely unknown. Hence, we conducted this study to explore potential roles and underlying oncogenic mechanisms for SNHG17 in ESCC progression. Results demonstrated SNHG17 to be markedly upregulated in ESCC. Knockdown of SNHG17 significantly suppressed ESCC cell proliferation, invasion, and epithelial-mesenchymal transition in vitro and tumor growth in vivo. Online database software analysis found miR-338-3p to interact with SNHG17 with the level of miR-338-3p negatively correlated with SNHG17 levels in ESCC samples. Further, miR-338-3p was found to directly target SRY-box transcription factor 4 (SOX4) in ESCC cells. Mechanistic analysis suggested that SNHG17 acts as an endogenous "sponge" competing with miR-338-3p to regulate SOX4, thereby promoting tumor progression. These results suggest that these molecular interactions may be potential therapeutic targets for ESCC.

Chen W ，Wang L ，Li X ，Zhao C ，Shi L ，Zhao H ，Huang C ... -  《Cell Death & Disease》

Long noncoding RNA SNHG12 induces proliferation, migration, epithelial-mesenchymal transition, and stemness of esophageal squamous cell carcinoma cells via post-transcriptional regulation of BMI1 and CTNNB1.

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors around the world. Numerous studies have revealed the function of long noncoding RNAs (lncRNAs) in cancers, including ESCC. In this study, lncRNA small nucleolar RNA host gene 12 (SNHG12), mainly distributed in ESCC cell cytoplasm, was overexpressed in ESCC specimens and CD133+ cells. In CD133- ESCC cells, SNHG12 overexpression promoted cell proliferation, migration, epithelial-mesenchymal transition (EMT), and stemness and SNHG12 silencing led to opposite results. Furthermore, SNHG12 sequestered miR-6835-3p and induced the proto-oncogene, polycomb ring finger (BMI1). SNHG12 also enhanced the stability of CTNNB1, the mRNA encoding β-catenin, via recruiting insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) in ESCC. Rescue assays indicated that CTNNB1 and BMI1 were targets for SNHG12 to regulate ESCC cell proliferation, migration, EMT, and stemness. Furthermore, SOX4 (sex-determining region Y-box 4) bound with the SNHG12 promoter to transcriptionally activate SNHG12 in ESCC. Finally, in vivo data showed SNHG12 knockdown retarded tumorigenesis and metastasis in ESCC. In summary, SNHG12 induces proliferation, migration, EMT, and stemness of ESCC cells via post-transcriptional regulation of BMI1 and CTNNB1, indicating that targeting SNHG12 might be a novel target for ESCC treatment.

Wu D ，He X ，Wang W ，Hu X ，Wang K ，Wang M ... -  《-》

SNHG17, as an EMT-related lncRNA, promotes the expression of c-Myc by binding to c-Jun in esophageal squamous cell carcinoma.

Dysregulation of long noncoding RNA SNHG17 is associated with the occurrence of several tumors; however, its role in esophageal squamous cell carcinoma (ESCC) remains obscure. The present study demonstrated that SNHG17 was upregulated in ESCC tissues and cell lines, induced by TGF-β1, and associated with poor survival. It is also involved in the epithelial-to-mesenchymal transition (EMT) process. The mechanism underlying SNHG17-regulated c-Myc was detected by RNA immunoprecipitation, RNA pull-down, chromatin immunoprecipitation, and luciferase reporter assays. SNHG17 was found to directly regulate c-Myc transcription by binding to c-Jun protein and recruiting the complex to specific sequences of the c-Myc promoter region, thereby increasing its expression. Moreover, SNHG17 hyperactivation induced by TGF-β1 results in PI3K/AKT pathway activation, promoting cells EMT, forming a positive feedback loop. Furthermore, SNHG17 facilitated ESCC tumor growth in vivo. Overall, this study demonstrated that the SNHG17/c-Jun/c-Myc axis aggravates ESCC progression and EMT induction by TGF-β1 and may serve as a new therapeutic target for ESCC.

Shen S ，Liang J ，Liang X ，Wang G ，Feng B ，Guo W ，Guo Y ，Dong Z ... -  《-》

Silencing of Long Noncoding RNA SNHG6 Inhibits Esophageal Squamous Cell Carcinoma Progression via miR-186-5p/HIF1α Axis.

Du F ，Guo T ，Cao C 《-》

Exosomal lncRNA ZFAS1 regulates esophageal squamous cell carcinoma cell proliferation, invasion, migration and apoptosis via microRNA-124/STAT3 axis.

Li Z ，Qin X ，Bian W ，Li Y ，Shan B ，Yao Z ，Li S ... -  《JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH》